• Journal of The Korean Society of Grassland and Forage Science
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• v.42 no.3
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• pp.208-214
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• 2022

Drought stress is a condition that occurs frequently in the field, it reduces of the agricultural yield of field crops. The aim of the study was to screen drought-adapted genotype of Italian rye grass. The experiments were conducted between the two Italian ryegrass (Lolium multiflorum L.) cultivars viz. Hwasan (H) and Kowinearly (KE). The plants were exposed to drought for 14 days. The results suggest that the morphological traits and biomass yield of KE significantly affected by drought stress-induced oxidative stress as the hydrogen peroxide (H₂O₂) level was induced, while these parameters were unchanged or less affected in H. Furthermore, the cultivar H showed better adaptation by maintaining several physiological parameter including photosystem-II (Fv/Fm), water use efficiency (WUE) and relative water content (RWC%) level in response to drought stress. These results indicate that the cultivar H shows improved drought tolerance by generic variation, improving photosynthetic efficiency and reducing oxidative stress damages under drought stress. These findings can be useful to the breeder and farmer for improving drought tolerance in Italian rye grass through breeding programs.

• Mycobiology
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• v.42 no.1
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• pp.52-58
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• 2014

A nucleoside diphosphate-linked moiety X (Nudix) hydrolase-like gene, YSA1, has been identified as one of the gromwell plant extract-responsive genes in Cryptococcus neoformans. Ysa1 is known to control intracellular concentrations of ADP-ribose or O-acetyl-ADP-ribose, and has diverse biological functions, including the response to oxidative stress in the ascomycete yeast, Saccharomyces cerevisiae. In this study, we characterized the role of YSA1 in the stress response and adaptation of the basidiomycete yeast, C. neoformans. We constructed three independent deletion mutants for YSA1, and analyzed their mutant phenotypes. We found that ysa1 mutants did not show increased sensitivity to reactive oxygen species-producing oxidative damage agents, such as hydrogen peroxide and menadione, but exhibited increased sensitivity to diamide, which is a thiol-specific oxidant. Ysa1 was dispensable for the response to most environmental stresses, such as genotoxic, osmotic, and endoplasmic reticulum stress. In conclusion, modulation of YSA1 may regulate the cellular response and adaptation of C. neoformans to certain oxidative stresses and contribute to the evolution of antifungal drug resistance.

• Journal of Dairy Science and Biotechnology
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• v.38 no.3
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• pp.134-141
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• 2020

Oxidative stress is a cascade reaction characterized by a significant increase in the amount of oxidized components. Free radicals produced by oxidative stress are one of the common features in several experimental models of disease, and contribute to wide range of neurodegenerative diseases, including Alzheimer's disease. Iron (II) species can participate in the Fenton, and Fenton-like reactions, to react with hydrogen peroxide and generate hydroxyl radical. As iron accumulation and oxidative stress are associated with the pathological progression of neurodegenerative diseases, iron chelation and antioxidant therapies have become strategies to combat these diseases. Due to the complexity of the redox system in vivo, a multifaceted approach may be an attractive therapeutic strategy. Further investigations are highly expected for the prevention and treatment of neurodegenerative diseases in future.

• Biomolecules & Therapeutics
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• v.17 no.4
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• pp.395-402
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• 2009

Insulin appears to play a role in brain physiology, and disturbances of cerebral insulin signalling and glucose homeostasis are implicated in brain pathology. The objective of the present study was to investigate the protective effects of insulin under conditions of oxidative stress induced by hydrogen peroxide ($H_2O_2$) in C6 glial cells. Insulin at concentration of $10^{-7}$ M could prevent 12 h $H_2O_2$-induced cell death. The formation of reactive oxygen species (ROS), nitric oxide (NO) and 2-thiobarbituric acid-reactive substances (TBARS) were significantly scavenged by insulin pre-treatment in C6 glial cells after $H_2O_2$-induced oxidative stress. Insulin significantly stimulated the phosphorylation of Akt in the cells and the activation of Akt was maintained in response to insulin under $H_2O_2$ incubation for 12 h. In conclusion, these results provide evidence that insulin acts as a free radical scavenger and stimulating Akt activity. These data suggest that insulin may be effective in degenerative diseases with oxidative stress.

• Proceedings of the Korean Environmental Health Society Conference
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• 2004.06a
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• pp.178-181
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• 2004

Di-n-butyl phthalate (DBP) is used extensively in the plastic industry and has been known as an environmental hormone (endocrine disruptor). Present study was undertaken to examine whether DBP can induce oxidative stress in mice. In this study, oxidative stress was measured in terms of the modification of lipid peroxidation and gamma-glutamyltranspeptidase (${\gamma}-GT$) activity. The activity of ${\gamma}-GT$, the level of lipid peroxidation and serum toxicity index were measured in male ICR mice after treatment with DBP (5 g/kg, po). Administration of DBP was found to significantly increase the level of lipid peroxidation approximately 2 fold in liver. The activity of ${\gamma}-GT$ in the liver of DBP-exposed animals was also increased approximately 2.5 fold. However, DBP did not alter the parameters for hepatotoxicity and nephrotoxicity such as alanine aminotransferase (ALT), aspartate aminotransferase (AST) and creatinine. These results indicate that DBP can induce oxidative stress in mice. The ${\gamma}-GT$ activity is considered to be increased as one of the adaptive defense mechanisms to oxidative stress induced by DBP.

• The Journal of Internal Korean Medicine
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• v.32 no.2
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• pp.188-202
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• 2011

Objectives : Oxidative stress seems to play a major role in mechanisms by which ethanol causes liver injury. Previous studies have shown that treatment with Chungganhaeju-tang (Qingganjiejiu-tang, CGHJT) has protective effects on alcoholic liver disease. The aim of this study was to investigate the effects of Chungganhaeju-tang on oxidative stress. Materials and Methods : In vitro, we evaluated the inhibitory activities of CGHJT on DPPH (1,1-diphenyl-2-picryl-hydrazyl), xanthine oxidase, trypsin, and hyaluronidase, and measured cell viability, and proliferation. In the cell culture model, we measured the activities of superoxide dismutase (SOD), and catalase (CAT) after CGHJT treatment in C34 and E47 cell lines, HepG2 cells transfected with/without the cytochrome P450 2E1 (CYP2E1) gene. In vivo, we measured malondialdehyde levels in the liver tissue and alcohol concentration in the blood. Results : CGHJT showed significant free radical scavenging activity against DPPH and xanthine oxidase in the in vitro study, and increased cell viability, proliferation, and activities of superoxide dismutase, catalase in C34 and in E47 cell lines. CGHJT reduced malondialdehyde levels and blood alcohol concentration in vivo, as well. Conclusions : This study suggests that CGHJT has antioxidant effects on oxidative stress by reducing lipid peroxidation and inhibiting the ethanol induced suppression of antioxidant enzyme activities.

• Preventive Nutrition and Food Science
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• v.15 no.1
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• pp.7-13
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• 2010

We investigated whether the fermented soymilk extract (FSE) has protective effects against high glucose-induced oxidative stress in human umbilical vein endothelial cells (HUVECs). FSE was prepared via fermentation of soymilk with Bacillus subtilis followed by methanol extraction. To determine the protective effect of FSE, oxidative stress was induced by exposing of HUVECs to the high glucose (30 mM) for 48 hr. Exposure of HUVECs to high glucose for 48 hr resulted in a significant (p<0.05) decrease in cell viability, catalase, SOD and GSH-px activity and a significant (p<0.05) increase in intracellular ROS level and thiobarbituric acid reactive substances (TBARS) formation in comparison to the cells treated with 5.5 mM glucose. However, at concentration of 0.1 mg/mL, FSE treatment decreased intracellular ROS level and TBARS formation, and increased cell viability and activities of antioxidant enzymes including catalase, SOD and GSH-px in high glucose pretreated HUVEC. These results suggest that FSE may be able to protect HUVECs from high glucose-induced oxidative stress, partially through the antioxidative defense systems.

• BMB Reports
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• v.47 no.9
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• pp.524-529
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• 2014

Oxidative stress and inflammation are common to many pathological conditions. Defense mechanisms protect cells from oxidative stress, but can become over-activated following injury and inflammation. NF-${\kappa}B$ and Nrf2 transcription factors regulate proinflammatory and antioxidant gene expression, respectively. Studies have shown that many natural dietary compounds regulate NF-${\kappa}B$ and Nrf2, preventing inflammation and oxidative stress. Here, we report major compounds of Prunella vulgaris var. lilacina such as rosmarinic acid, oleanolic acid, ursolic acid and caffeic acid as a potential therapeutic for oxidative stress and inflammation. The major compounds exhibited high anti-inflammatory activity, inhibiting NO, PGE2 production, NF-${\kappa}B$ expression and activating Nrf2 expression. In addition, we examined the effect of major compounds on MafK expression. Among the compounds, oleanolic acid significantly decreased MafK expression and MafK-mediated p65 acetylation. These findings suggest that oleanolic acid as NF-${\kappa}B$ inhibitors can potentially be used in therapeutic applications for the treatment of oxidative stress-induced diseases.

• Toxicological Research
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• v.22 no.3
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• pp.253-266
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• 2006

Bone is a dynamic tissue that is constantly being remodelled. Resolution of bone and formation of new bone are closely linked, so that bone mass remains constant. With age, this process becomes unlinked with an imbalance in bore resorption and formation that results in a net loss of bone. Especially, osteoporosis is a disease characterized by low bone mass with age. One form of aging-related primary osteoporosis is postulated with the reduction of circulating estrogen, rapid bone loss occurs as a result of enhanced bore remodelling with an excess of resorption over bore formation. The oxidative stress is also involved in the pathogenesis of osteoporosis. Oxidative stress by cytokines, such as IL-a and TNF-${\alpha}$, inhibits osteoblast function in vitro and stimulates osteoblast apoptosis resulting in an imbalance in bore remodelling. The present article reviews the current perspectives on the interaction between bone remodelling and factors such as estrogen and oxidative stress, providing an interpretation of bone diseases in a view of molecular mechanisms.

• Nutrition Research and Practice
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• v.9 no.2
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• pp.144-149
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• 2015

BACKGROUND/OBJECTIVE: The aim of this study was to examine the effect of high dietary methionine (Met) consumption on plasma and hepatic oxidative stress and dyslipidemia in chronic ethanol fed rats. MATERIALS/METHODS: Male Wistar rats were fed control or ethanol-containing liquid diets supplemented without (E group) or with DL-Met at 0.6% (EM1 group) or 0.8% (EM2 group) for five weeks. Plasma aminothiols, lipids, malondialdehyde (MDA), alanine aminotransferase (ALT), and aspartate aminotransferase were measured. Hepatic folate, S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH) were measured. RESULTS: DL-Met supplementation was found to increase plasma levels of homocysteine (Hcy), triglyceride (TG), total cholesterol (TC), and MDA compared to rats fed ethanol alone and decrease plasma ALT. However, DL-Met supplementation did not significantly change plasma levels of HDL-cholesterol, cysteine, cysteinylglycine, and glutathione. In addition, DL-Met supplementation increased hepatic levels of folate, SAM, SAH, and SAM:SAH ratio. Our data showed that DL-Met supplementation can increase plasma oxidative stress and atherogenic effects by elevating plasma Hcy, TG, and TC in ethanol-fed rats. CONCLUSION: The present results demonstrate that Met supplementation increases plasma oxidative stress and atherogenic effects by inducing dyslipidemia and hyperhomocysteinemia in ethanol-fed rats.